MODES OF DEATH: According to Bichat, there are three modes of death, depending on whether death begins in one or other of the three systems, irrespective of what the remote causes of death may be. These modes are: Asphyxia, Coma and Syncope.
According to Gordon (1944) the stoppage of vital functions depends upon tissue anoxia. Anoxia means lack of oxygen’. It may be:
(1) Anoxic anoxia: In this type, oxygen cannot reach the blood, because of lack of oxygen in the lungs. This occurs:
(2) Anaemic anoxia: In this type, oxygen-carrying capacity of the blood is reduced, e.g., acute massive hemorrhage, poisoning by carbon monoxide, chiorates, nitrates, coaltar derivatives.
(3) Stagnant anoxia: In this type, impaired circulation results in a reduction of oxygen delivery to the tissues, e.g., heart failure, embolism and shock.
(4) Histotoxic anoxia: In this type, the enzymatic processes by which the oxygen in the blood is used by the tissues are blocked, e.g., acute cyanide poisoning. Anoxic anoxia due to lack of oxygen in the inspired air or mechanical obstruction to respiration is usually known as asphyxia or mechanical asphyxia. These four types of anoxia ultimately lead to cardiac failure and death.
Normal levels of oxygen in arterial blood (P02) is 90 to 100 mm. Hg at 30 years and 65 to 80 at 60 years and above. Reduction to 60 mm Hg results in hypoxia. At 40 mm Hg, there is severe hypoxia, and death may occur at 20 mm Hg.
Asphyxia is a condition caused by interference with respiration, or due to lack of oxygen in respired air, due to which the organs and tissues are deprived of oxygen (together with failure to eliminate C02), causing unconsciousness or death. Nervous tissues are affected first by deficiency of oxygen and their functions are disturbed even by mild oxygen lack.
The term asphyxia indicates a mode of dying, rather than a cause of death. The neurons of the cerebral cortex will die in 3 to 7 minutes of complete oxygen deprivation, and the other nerve cells remain alive for a little longer time. Irreversible cortical damage may occur if oxygenated blood fails to perfuse the brain up to 7 to 9 minutes. Subnormal oxygen in the blood supply to the brain causes rapid unconsciousness.
In all forms of asphyxia, heart may continue to beat for several minutes after stoppage of respiration. The rule of thumb is: breathing stops within twenty seconds of cardiac arrest, and heart stops within twenty minutes of stopping of breathing. If the heart functions for several minutes after stoppage of breathing, the weight of the lungs may increase to 450 to 500 g.
Types and Causes:
(1) Mechanical: In this the air-passages are blocked mechanically.
(2) Pathological: In this, the entry of oxygen to the lungs is prevented by disease of the upper respiratory tract or of the lungs, e.g., bronchitis, acute edema of the glottis, laryngeal spasm, tumors and abscess. Paralysis of the respiratory muscles may result from acute poliomyelitis.
(3) Toxic: Poisonous substances prevent the use of oxygen.
(6) Postural asphyxia: This is seen where an unconscious or stuporous person, either from alcohol, drugs or disease, lies with the upper half of the body lower than the remainder.
(7) Latrogenic is associated with anesthesia.
When the neck is compressed, occlusion of jugular veins prevents venous drainage from the head, but the arterial supply continues through the carotid and vertebral arteries. When the air-passages are occluded, the impaired oxygenation in the lungs causes decrease in the oxygen content of arterial blood.
Reduction in oxygen tension causes capillary dilation which is followed by stasis of blood in the dilated capillaries and venules, which produces capillo-venous engorgement. This blood stasis causes congestion of organs, and venous return to the heart is diminished leading to anoxia, which causes capillary dilatation and the vicious cycle goes on.
Petechial hemorrhages are caused due to raised venous pressure from impaired venous return resulting in over distension and rupture of venules, and not to hypoxia of the vessel walls. A minimum of 15 to 30 seconds is required to produce congestion and petechiae. Petechiae vary in size from 0.1 to 2 mm. If larger than this they are called ecchyinoses. Sometimes, large hemorrhages are seen on upper chest and back of the body.
Petechiae are seen in the skin, selerae, conjunctivae, outer and inner surfaces of the eyelids, and on the mucosal surfaces in the mouth. The haemorrhages may be found in the substance of the viscera, but they are readily seen in serous membranes, particularly in the visceral pleura and pericardium.
Petechiae are rarely seen in the parietal pleura and peritoneum except in hemorrhagic diatheses. The increased capillary and venous permeability causes transudation of fluid into tissues. In the early stages, the transudation is followed by increased lymph drainage and edema does not develop. If the hypoxia continues, edema of the tissues develops.
Edema of the lungs is common, and is usually caused due to combination of hypoxia and raised pulmonary vessel pressure, and its presence indicates struggle for survival for a time. Edema of the brain occurs due to back- pressure and hypoxia. Generalized edema is not prominent. Congestion and edema are non-specific and result due to obstructed venous return.
When the neck is compressed, the face, lips, and tongue become swollen and reddened. Cyanosis (bluish colour of the skin, mucous membranes and internal organs) follows congestion of the face, as venous blood containing much reduced haemoglobin after perfusing the head and neck becomes bluer. If the airway is blocked, the impaired oxygenation in the lungs causes decrease in the oxygen content of the arterial blood, which causes darkening of all organs and tissues and will increase the cyanosis of the face.
Oxygenated blood is bright-red. It becomes purplish-blue when oxygen is given up. Cyanosis is marked in the skin where hypostatic livid stains develop, and lips, ears, tip of nose, fingernails, cheeks, and internally the lungs, liver, spleen, kidneys and meninges are cyanosed. More than 5g/ 100 ml of whole blood should be in the form of reduced hemoglobin regardless of the total hemoglobin concentration.
The essential cause of cyanosis is diminished oxygen tension in the blood with a rise in proportion of the reduced haemoglobin. Methaemoglobin and sulphhaemoglobin also cause cyanosis. Increased capillary permeability probably results from a combination of stasis and hypoxia.
When carotid arteries are obstructed, intensity of cerebral, facial, and orbital petechiae are much less prominent, than what is seen in cases where venous obstruction predominates. In sudden complete carotid obstruction, facial pallor can be striking. Bleeding from the ear and nose occurs when the back-pressure is severe to rupture small superficial vessels.
Dilatation of the heart chambers on the right side and fluidity of the blood in deaths due to asphyxia are absolete and should be disregarded. This is seen in any type of congestive death, including primary heart failure from many diseases, and is due to the generalized rise in venous and intracardiac pressure. Distension of the atria and ventricles is a common postmortem finding and may result from secondary muscular flaccidity.
The light lungs (about 300 gm.) are more compatible with sudden rhythm disturbance and cessation of the action of the heart. Heavier lungs (450 to 500 gm. or more) indicate cessation of respiration with continuance of the heartbeat for several minutes.
(1) Partial disruption of alveolar septa with distinctive hemorrhage within the alveoli and intra-alveolar oedema fluid.
(2) Brick-red discoloration of nerve cells in cerebral cortex seen in stained neurological sections, Pallor and vacuolar degeneration of Purkinje cells in the cerebellum.
(3) Vacuolar degeneration of liver cells in prolonged suffocation.
Asphyxia is not a pathological entity, and cannot be clearly recognized from morbid anatomical findings alone.
The triad of (1) cyanosis, (2) facial, palpebral, bulbar, subpleural and subepicardial petechiae, (3) visceral congestion, are all due to raised venous pressure.
They are merely consistent with, but not diagnostic of asphyxia from anoxic anoxia. Reliable local indications of fatal obstructing trauma must be demonstrated to establish that death occurred from mechanical asphyxia. Parenchymatous degenerative changes develop in rapid hypoxic and rapid anoxic deaths, but they are non-specific.
Postmortem Fluidity of the Blood
Shortly after death the blood is usually fluid, and when it is removed from the body, it undergoes spontaneous coagulation. If the autopsy is done a few hours after death, the blood may be partly clotted and partly fluid. Uncoagulable fluid blood is normally present in the limb vessels and often in the heart of any healthy person who dies suddenly from any cause. It does not give any indication of the cause of death. In most deaths from asphyxia, the blood is fluid and incoagulable.
The postmortem fluidity of the blood is due to presence of fibrinolysins, liberated from the vascular endothelium. Fibrinolysin activation occurs due to release of plasminogen activator, through the receptors on the vascular wall for various vasoactive materials that increase during the agonal period.
Fibrinolysis is also activated by the leakage of plasminogen-activator due to increased permeability, and to degeneration and necrosis of the cell membrane, as a result of excessive acidosis after death. It is considered that the lysin is adsorbed on to the thrombi, and released into solution when the fibrin is lysed.
Under certain conditions, the fibrinolysin may be so active that fibrin is destroyed as rapidly as it is produced, and postmortem clots never develop in the vessels. In other cases, thrombi are formed, but they undergo lysis. In deaths associated with infection and cachexia, and slow natural death, fibrinolysins may fail to develop and abundant clots are seen in the heart and in the limb vessels.
The concentration of circulating fibrinolysins is more in healthy persons, which is further increased during exercise and also due to emotional stress. Therefore, blood is fluid in young persons dying of unnatural causes.
Postmortem clotting of blood in the heart and venous system is a most erratic process. The condition of the blood at autopsy depends upon the concentration of fibrinolysin, and the rate of intravascular coagulation after death. The blood is likely to be fluid, when the fibrinolysin is active and the rate of coagulation is slow. Postmortem thrombi are formed when the firbrinolysin is less active, and the rate of coagulation is rapid.
(1) STAGE OF DYSPNOEA: The excess of carbon dioxide in the blood stimulates the respiratory center. The respiratory movements become increased in rate and amplitude, blood pressure is increased, pulse rate increases and there is slight cyanosis.
(2) STAGE OF CONVULSIONS: The effort to breathe is mostly expiratory, the face is deeply congested, blood pressure is increased, pulse is fast, veins in the neck become swollen. There are frequently convulsions which cease as the victim becomes insensible and the reflexes are abolished.
(3) STAGE OF EXHAUSTION: The respiratory center is paralyzed, the muscles become flaccid. There is complete insensibility, reflexes are lost and the pupils are widely dilated. The breathing is gasping, mostly inspiratory with long intervals between the gasps.
The blood pressure falls, muscles relax, respiration ceases, and death takes place. The pulse is imperceptible, but the heart may continue to beat for some minutes after respirations have ceased. The three stages last for 3 to 5 minutes before death takes place.
External: Postmortem hypostasis is well developed. The face is either pale in slow asphyxia, or distorted, congested, often cyanosed and purple, and sometimes swollen and oedematous. Ears and fingernails are bluish. The eyes are prominent, the conjunctivae are congested and the pupils are dilated. The tongue is protruded in most cases, and frothy and bloody mucus escapes from the mouth and nostrils.
Petechial hemorrhages, known as Tardien spots are most marked where for mechanical reasons, capillary congestion is most prominent. Their distribution lies above the level of obstruction. They appear commonly as a rash-like shower in the scalp, eyelids and face in hanging and strangulation and in the zone above the level of compression in traumatic asphyxia.
A hand lens is useful to identify petechial hemorrhages. They are produced by simple mechanical obstruction to the venous return of blood from the parts, resulting in acute rise in venous pressure and over distension and rupture of thin walled peripheral venules, especially in lax, unsupported tissues, such as forehead, skin behind the ears, eyelids, circumoral skin, conjunctivae and sclerae, neck, buccal mucosa, epiglottis, visceral pleura, pericardium, thymus and rarely in the serosa of the bowel (Fig. 6-2to4). In many cases unconsciousness can occur in several seconds.
Internal: The blood is fluid and dark, because of increased amount of CO2. The large veins are full of blood. Vessels may burst in the eardrum and in the nose causing bleeding. The larynx and trachea are usually congested, and contain a varying amount of slightly frothy mucus. The lungs are dark and purple. If the back pressure persists, there is exudation of serous or serosanguineous fluid in the alveoli, producing edema.
The amount of pulmonary edema, does not indicate the time interval between injury and death. Accumulation of fluid in the posterior and dependent parts of the lungs after death, should not be mistaken for pulmonary edema. Some of the marginal portions of the lungs may show emphysematous changes. The abdominal viscera show marked venous congestion. The brain is often congested. The cranial sinuses are usually filled with dark blood.
Tardieu spots are numerous where the capillaries are least firmly supported, as in subconjunctival tissues and under the pleural and pericardial membranes but they can appear almost anywhere if the degree of congestion and cyanosis is sufficient. Tardieu spots are usually round, dark, and well-defined, varying in size from a pins head to two mm. They may occur as isolated minute hemorrhages or present in large numbers, and at times fuse to form patches of red color, especially at the back of the heart.
They are numerous in the region of auriculoventricular junction and the lower lobes and the interlobar fissure of the lungs and thymus. In the brain, petechiae occur in the white matter, and there may be larger patches of bleeding in the sub-arachnoid space, because of acute venous engorgement. Often profuse petechiae and ecchymoses are seen under the scalp due to the same mechanism.
The time taken for these various signs to occur depends on the circumstances, from a few seconds to several minutes. Petechiae and ecchymoses are common non-specific autopsy findings and may be seen in many non-asphyxial deaths beneath the pericardium, pleura, interlobar fissures and around the hilum. Petechiae are likely to occur in association with cyanotic congestion and may not be visible until the area is drained of blood during autopsy.
Sometimes, it is difficult to distinguish petechiae from the cut ends of congested vessels, especially in the brain. Microscopic examination will confirm the nature of hemorrhage. Cutaneous and visceral petechiae, especially the latter can appear and enlarge as a postmortem phenomenon. They are seen on the front or back of corpses who have died from causes other than mechanical asphyxia.
They are often seen in normal postmortem hypostasis, especially where the mode of death was congestive as in many types of natural heart disease. As such petechiae are highly unreliable indicators of an asphyxial process.
The natural diseases which produce hemorrhages in the skin include bacterial endocarditis, meningococcal septicaemia and blood dyscrasias, especially purpura and haemophilia, and also in deaths from coronary thrombosis, acute heart failure, secondary shock, and rapid anoxia.
Petechiae can be seen following any severe increase in intrathoracic pressure including asthmatic attack, heart failure, respiratory failure, straining at stool, and soon after delivery. These conditions produce relatively large haemorrhages which tend to combine. Their distribution is general, whereas Tardieu spots are present above the level of obstruction.
Asphyxia causes vomiting due to medullary suboxia, due to which the air-passages may be filled at the end of asphyxial event by the inhaled vomit. This finding especially in infants, shoud not be assumed to be the cause of asphyxia; it is more likely to be the result. About 20 to 25% of all individuals aspirate food agonally whatever may be the cause of death.
There are variations in the intensity of asphyxial signs. When the asphyxial process is slight and prolonged, the congestive element will be diminished; when intense and short, lividity and congestion are marked. If, during the process of asphyxia, heart failure occurs before respiratory failure, the asphyxial signs may be less marked, depending at which stage in the asphyxial process, the cardiac arrest occurred. Sometimes, the findings are not sufficient to use an accurate term, and the cause of death has to be given within a broad framework, such as “consistent with asphyxia”.
In the presence of putrefaction, mechanical asphyxia is indicated by presence of petechial hemorrhages under the eyelids, conjunctivae, sclerae and facial skin.
The higher cortical centers suffer first from hypoxic injury, followed by basal ganglia and ultimately the vegetative centres, which explain delayed deaths. Such delayed deaths usually follow periods of unconsciousness, resulting from anoxic cerebral damage and subsequent hypostatic pneumonia.
Other lethal sequelae include, massive subcutaneous and mediastinal emphysema from tracheal and laryngeal lacerations, or occlusion of airway due to oedematous or hemorrhagic swelling of pharyngeal tissues or the aryepiglottic folds. When death occurs hours, days or weeks after the asphyxial episode, the proximate cause of death is the traumatic incident.
It is a state of unarousable unconsciousness determined by the absence of any psychologically understandable response to external stimuli or inner need. It involves the central portion of the brain stem. Coma is a clinical symptom and not a cause of death.
(1) Compression of the brain, e.g., effusion of blood on or in the brain, inflammation, abscess or neoplasni of brain.
(2) Drugs; opium, hypnotics, cocaine, alcohol, anesthetics, cyanide, atropine, phenol, oxalic acid, CO, etc.
(3) Metabolic disorders and infections: uremia, cholaemia, eclampsia, diabetes, pneumonia, infectious fevers, heat stroke, etc.
(4) Other causes: embolism and thrombosis in the cerebral vessels, epilepsy, hysteria, etc.
Injuries or disease of the brain may be present as noted in the causes of coma. The lungs, brain and the meninges are congested. Splanchnic pooling of blood occurs.
Syncope is sudden stoppage of action of the heart, which may prove fatal. This term is also not used as a cause of death. Syncope or fainting is due to vasovagal attacks resulting from reflex parasympathetic stimulation. Syncope is caused by reflex bradycardia or asystole, or by reflex splanchnic vasodilation. Due to the acute reflex circulatory changes, blood pressure falls suddenly causing cerebral anemia and rapid unconsciousness. Recovery is common.
(1) Anemia due to sudden and excessive hemorrhage.
(2) Asthenia from deficient power of heart muscle as in fatty degeneration of the heart, myocardial infarction and certain poisons.
(3) Vagal inhibition.
(4) Exhausting diseases.
The heart is contracted and the chambers are empty when death has occurred from anemia, but chambers contain blood when death occurs due to asthenia. The lungs, brain and abdominal organs are usually pale and the capillaries are congested. Splanchnic pooling of blood occurs.